He Yue, Chen Jie, Zhang Shu-Guang, Yuan Yuan-Sheng, Li Yan, Lv Hong-Bin, Gan Jin-Hua
Department of Ophthalmology, the Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan Province, China.
Department of Rheumatology and Immunology, the Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan Province, China.
Neural Regen Res. 2015 Mar;10(3):432-7. doi: 10.4103/1673-5374.153692.
Glaucoma, a type of optic neuropathy, is characterized by the loss of retinal ganglion cells. It remains controversial whether c-Jun N-terminal kinase (JNK) participates in the apoptosis of retinal ganglion cells in glaucoma. This study sought to explore a possible mechanism of action of JNK signaling pathway in glaucoma-induced retinal optic nerve damage. We established a mouse model of chronic ocular hypertension by reducing the aqueous humor followed by photocoagulation using the laser ignition method. Results showed significant pathological changes in the ocular tissues after the injury. Apoptosis of retinal ganglion cells increased with increased intraocular pressure, as did JNK3 mRNA expression in the retina. These data indicated that the increased expression of JNK3 mRNA was strongly associated with the increase in intraocular pressure in the retina, and correlated positively with the apoptosis of retinal ganglion cells.
青光眼是一种视神经病变，其特征是视网膜神经节细胞丢失。c-Jun氨基末端激酶（JNK）是否参与青光眼患者视网膜神经节细胞的凋亡仍存在争议。本研究旨在探讨JNK信号通路在青光眼所致视网膜视神经损伤中的可能作用机制。我们采用激光烧灼法减少房水，建立了慢性高眼压小鼠模型。结果显示，损伤后眼组织出现明显的病理变化。视网膜神经节细胞的凋亡随着眼压升高而增加，视网膜中JNK3 mRNA的表达也随之增加。这些数据表明，JNK3 mRNA表达的增加与视网膜眼压升高密切相关，并与视网膜神经节细胞的凋亡呈正相关。
